Mechanism of Crosstalk between m6A Modification and Epigenetic Regulation
Crosstalk ID
M6ACROT00550
[1], [2], [3]
RNA modification MIR210 MIR210 ADAR Methylation : modification sites Indirect Enhancement m6A modification SMAD4 SMAD4 YTHDF2 : m6A sites
m6A Modification:
m6A Regulator YTH domain-containing family protein 2 (YTHDF2) READER
m6A Target Mothers against decapentaplegic homolog 4 (SMAD4)
Epigenetic Regulation that have Cross-talk with This m6A Modification:
Epigenetic Regulation Type RNA modification (RNAMod)  >> Adenosine-to-Inosine editing (A-to-I)
Epigenetic Regulator Interferon-inducible protein 4 (ADAR1) WRITER View Details
Regulated Target MicroRNA 210 (MIR210) View Details
Crosstalk Relationship A-to-I  →  m6A Enhancement
Crosstalk Mechanism RNA modification indirectly impacts m6A modification through downstream signaling pathways
Crosstalk Summary ADAR1 interacts with MicroRNA 210 (MIR210), increasing it's A-to-I level and promoting its physical interaction with Mothers against decapentaplegic homolog 4 (SMAD4), which was regulated by YTHDF2-mediated m6A modification.
In-vitro Model
HSC (Hematopoietic stem cell)
HN4 Clear cell renal cell carcinoma Homo sapiens CVCL_IS30
CAL-27 Tongue squamous cell carcinoma Homo sapiens CVCL_1107
References
Ref 1 Suppression of m(6)A reader Ythdf2 promotes hematopoietic stem cell expansion. Cell Res. 2018 Sep;28(9):904-917. doi: 10.1038/s41422-018-0072-0. Epub 2018 Jul 31.
Ref 2 ADAR1 promotes the epithelial-to-mesenchymal transition and stem-like cell phenotype of oral cancer by facilitating oncogenic microRNA maturation. J Exp Clin Cancer Res. 2019 Jul 17;38(1):315. doi: 10.1186/s13046-019-1300-2.
Ref 3 miR-210 Participates in Hepatic Ischemia Reperfusion Injury by Forming a Negative Feedback Loop With SMAD4. Hepatology. 2020 Dec;72(6):2134-2148. doi: 10.1002/hep.31221. Epub 2020 Sep 2.